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Module 2 > Respiratory Viral Infections > Flashcards

Respiratory Viral Infections Flashcards

1
Q

Why is there a global potential of new respiratory viral epidemics?

A

viruses mutate and evolve fast; respiratory viruses spread fast by bird or human flight; widely zoonotic; difficult to contain

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2
Q

How does the incidence of respiratory illnessses per person per year change with age?

A

declines over the course of a lifetime with a peak in the early 20s

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3
Q

What is the percentage of respiratory infections caused by viruses?

A

75%

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4
Q

What is the type of genetic info in RSV?

A

RNA

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5
Q

What protein in the virus determines the viral tropism?

A

viral coat

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6
Q

What is the suffix of all viral families?

A

viridae

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7
Q

What is the suffix of a viral genus?

A

virus

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8
Q

What type of virus has quasispecies?

A

RNA viruses

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9
Q

Give examples of DNA viruses?

A

poxviruses; herpesviruses

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10
Q

How are DNA viruses adapted to immune pressures?

A

mimicry

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11
Q

What is a quasispecies?

A

mutant viruses that develop as a virus replicates in a host

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12
Q

What is the envelope of virsues derived from?

A

host membrane- lipid

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13
Q

What is found on the outside of viruses that don’t have an evelope?

A

symmetrical protein capsid

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14
Q

Why is it difficult to block the replicative processes of viruses?

A

use the host’s biochemistry

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15
Q

Give an example of an infection which has acute viral infection then clearance?

A

flu

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16
Q

give an example of an infection which shows acute viral infection/clearance and re-infection?

A

RSV

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17
Q

Give an exmaple of a virus which shows slow chornic infection?

A

CMV

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18
Q

What is the general mechanism behind viral causes of oncogenesis?

A

an immune defense against viruses is apoptosis, thereofre viruses turn off this mechnism to survive, but this also results in cancer

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19
Q

What is viral culture?

A

growing virus in immortalised cell line

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20
Q

What family do the human rhinoviruses come under?

A

picornaviruses

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21
Q

What type of virus are the influenza viruses?

A

orthomyxoviruses

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22
Q

What are coronaviruses typically responsible for?

A

zoonotic transmission and epidemics

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23
Q

What viruses are paramyxoviruses?

A

RSV; parainfluenza

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24
Q

How many genes does RSV have?

A

10

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25
Q

What type of genome does RSV have?

A

ssRNA

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26
Q

Why is RSV able to reinfect?

A

stimulates poor immunological memory

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27
Q

What is the function of NS1 and NS2 in RSV?

A

non-structural proteins which have anti-interferon a and b activity

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28
Q

What is the function of N and P genes in RSV?

A

nucleoprotein and phosphoprotein- nucleocapsid proteins essential for transcriptional activity

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29
Q

What is the function of M gene in RSV?

A

matrix protein- viral assembly

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30
Q

What is the function of SH gene in RSV?

A

small hydrophobic protein- unkown function

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31
Q

What is the function of G gene in RSV?

A

glycoprotein- viral attachment to the cell

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32
Q

What is the function of F gene in RSV?

A

fusion protein- viral entry and syncytia formation

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33
Q

What is the function of M2 gene in RSV?

A

M2:1- transcription elongation factor; M2-2: regulation of viral transcription

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34
Q

What is the function of L gene?

A

nucleocapsid protein- RNA polymerase

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35
Q

How many strains of RSV are there?

A

2- A and B

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36
Q

What is RSV associated with in later life of infants it infects?

A

wheezing/astham (chicken and egg Q– are children more ;ikely to get RSV is predisposed to asthma; or does RSV change lungs)

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37
Q

What is the largest single cause of hsopitalisaiotn in infancy?

A

RSV

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38
Q

What disease does RSV cause in infants?

A

bronchiolitis

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39
Q

What age is the highest risk for RSV bronchiolotis?

A

1-6months

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40
Q

What are the 2 forms of surface glycoproteins on influenza?

A

neuraminidase (N) and haemagglutinin (H)

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41
Q

What is unique about the genome of influenza viruses compared with otehr respiratory viruses?

A

have a segmented genome

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42
Q

What is antigenic drift?

A

minor changes caused by point mutations- slow process – antibody no longer recognises

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43
Q

What is antigenic shift?

A

multiple alterations in antigenic makeup due to reassortment of genome segments; rapid process associated with pandemic outbreaks

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44
Q

Describe the pathogenicitiy of H5N1?

A

can replicate efficiently only in cells in the lower region of resp tract where the avianvirus receptor is prevalent- if gets into lower airways causes havoc but limited in its chances of getting there- mainly poultry workers

45
Q

Where were >70s not affected by H1N1?

A

similar virus in the 1960s so immunological memory

46
Q

Why is influenza difficult to prevent the transmission of?

A

very infecitous when asymptomatic

47
Q

How amny serotypes are there of human rhinoviruses?

A

> 100

48
Q

What is the second main cause of hospitalisation in children under 5 years?

A

parainfluenza

49
Q

What disease is parainfluenza assocaited with ?

A

croup

50
Q

What is the evidence that RSV disease isn’t caused by virus directly but immunopathology?

A

illness is after the peak viral load, SCID mice do not get normal RSV pathology, instead are overwhelmed by virus after WT mice have cleared infection

51
Q

What form does prophylaxis of viral infection take?

A

passive transfer of antibody to block disease

52
Q

When are antivirals particularly effective?

A

when viral pathogenesis/persistence is the problem

53
Q

Why would anti-RSV drug not work in acute infection?

A

by the time giving antivirals in response to symptosm , too late as viral peak has already happened, symptoms happeneing as result

54
Q

What is hte problem with tinkering with inflammation e.g anti-TNF?

A

very dependent upon timing as during peak viral load need to boost inflam whereas need to dampen inflammation during actual disease after viral peak

55
Q

What is the most common lab abnormality detected in viral infection?

A

hypoxamia

56
Q

What are the absolute indications for hospital referrals for acute bronchiolotis?

A

cyanosis or severe respiratory distress (RR>70; nasa flaring; grunting; chest wall recession); marked lethargy-poor feeding; respiratory distress preventing feeding (<50% usual intake in past 24 hours); apnoeic epsidoes; diagnostic uncertainty

57
Q

What pulse ox says a baby should be admitted?

A

<=92

58
Q

What is the first choice in control of viruses?

A

vaccination

59
Q

What is the treatment for bronchiolitis?

A

supportive- oxygen (intubation; CPAP; head box)’; fluids; +/- antibiotics; vasodilators and CS

60
Q

How many respiratory infections do children get per year on avergae?

A

5-6

61
Q

How many infants with respiratory viral infections will develop lower respiratory tract symptoms ?

A

1/3rd

62
Q

give examples of extrapulmonary manifestations of RSV infection?

A

seizures; hyponatraemia; cardiac arrhythmias; cardiac failure and hepatitis

63
Q

Which infants are at risk of severe LRTI?

A

premature and infants with congenital heart disease

64
Q

Give examples of neuraminidase inhibitors?

A

oseltamivir and zanamivir

65
Q

What is the benefit of neuraminidase inhibitors?

A

shortens symptoms by about 1 day and may reduce disease severity

66
Q

When are neuraminidase inhibitors helpful?

A

wihtin 48h of exposure or 36h after first symptoms- not in established influenza infection or sever LRTI

67
Q

Who should get neuraminidase inhibitors?

A

for children with chronic morbidity who are at an increased risk of sever influenza-induced disease

68
Q

What is ribavirin licensed for?

A

inhalation for severe RSV bronchiolitis

69
Q

What is a problem with ribavirin?

A

teratogenic

70
Q

Why has ribavirin provided little or no benefit?

A

once developed, the severe inflammation in RSV bronchioloitis may be maintained independetly of the presence of live RSV virions

71
Q

Which respiratory infections are cosrticosteroids helpful in?

A

croup

72
Q

What are the 4 main ways in which respiratory viruses are diagnosed?

A

virus culture; serology; immunofluorescen/antigen detection and nucleic acid/PCR based test

73
Q

What is serology?

A

blood is tested for either virus-specific antibodies or viral antigen by a functional assay

74
Q

What is the disadantage of both viral culture and serology?

A

cultures can take upto 10 days and the antibody response to viral infection can take 2 weeks (infection is often resolved before the infecitous agent is defined)– more useful in epidemiological studies

75
Q

Whati s the basis of antigen detection?

A

use of virus-specfic monoclonal antibodies

76
Q

Which viruses cause bronchiolotis?

A

influenza; adenovirus; human metapenumovirus; parainfluenza; rhinovirus and RSV

77
Q

What is the role of viral coinfection in bronchiolitis?

A

common-20% of cases; depends on whcih viruses coinfect together- increase in severesity with hMPV and RSV but not with RSV+ adenovirus/rhinovirus

78
Q

What is the benefit of knowledge of the infecting agent?

A

doesnt alter treatment but will reduce inappropriate antiboitic use and may allow cohorting of patients to reduce nosocomial infection

79
Q

What are the factors involvedi n likelihood of a respiratory tract infection?

A

age and exposure to infection

80
Q

What are the risk factors for severe RSV infection?

A

age when infected; increased exposure to an infectious agent; decreased body size; protection against virus due to breastfeeding and amount of IgG in breast milke; factors affecting lung function eg smoke and air pollution

81
Q

What are the factors related to increased exposure to an infectious agen?

A

siblin order; daycare attendance; birth season; hospitalisation and socioeconomic status

82
Q

Why does young age act as a metafactor?

A

age has an effect on the size of hte child- esp airway size; transmission dynamics; immune experience ; have smaller energy reserves and more likely to get exhausted by effort of breathing

83
Q

What is the ultimate cause of mortality in acute bronchiolitis?

A

exhuastion due to effort of breathing

84
Q

Polymrophisms in which genes of the innate immune system result in higher RSV susceptbility?

A

transcriptional regulator Jun; IFNa; nitric oxide synthase and the vitamin D receptor

85
Q

What are the 2 groups of genes important for changing the outcome following respiratory viral infection?

A

first group- involved in the magnitude and type of immune response e.g IL-4 or IL13; second- genes involved in control of viral load e.g TLR4; IL6; CD14

86
Q

Which TLRs detect viruses extracellularly?

A

TLR2,6 and 4 (mice deficient in TLR2/6 have increased RSV virla load)

87
Q

How does RSV interact with TLR4?

A

via its F protein

88
Q

What is the function of hte influenza virus NS1 protein?

A

concelas the viral genome from deetection

89
Q

How does RSV prevent RIG-I detection?

A

binds La antigen

90
Q

What is the effect of RSV on downstream signalling from PRRs?

A

inhibits IFN production; IRF3 activation is inhibited; although NF-kB increases following RSV (prevent apoptosis); IFNa receptor signalling by the JAK-STAT pathway

91
Q

How is the adaptive immune repsonse evaded by respiratory viruses priamrily?

A

mutation of viral proteins

92
Q

Which is the main respiratory virus that does not have an RNA genome?

A

adenovirus

93
Q

What effect does increasing glyosylation of the coat proteins of a virus have?

A

increased immune evasion

94
Q

What does influenza use to inhibit DC function?

A

haemagglutinin and NS1 proteins

95
Q

What suggests that lung damage caused by the virus is a key factor in pathology?

A

correlation bewteen viral load and disease severity; RSV cause inhibit cilia movement leading to airway blockade; study of infants who died of RSV showed presence of virus but not lymphocytes- however this might be due to immunodeficiency; RV causes cytotoxicity in vitro; inhibiting cytokein response had not effect on H5N1 pathogeneisis; IL-1 deficiency mice had worse pathology with influenza

96
Q

What evidence suggests that immunopathology is responsible for lung damage with respiratory infectiosn?

A

RSV-child who ided in crash had lots of lymphocytosis; RSV-infected HIV pos infants had icnreased viral shedding but decreased bronchiolitis; data shows patietns who died of SARS or H5N1 had cleared the virus; antiviral drugs did not alter disease outcome; RSV and RV are characterised by neutrophil infiltrate; IL-8 is upregulated in RSV bronchiolitis and asthmatics with RV

97
Q

What is the function of IL-8

A

main neutrophil chemosttractant

98
Q

What are the 2 main methods by which viral infection enhances bacterial infections?

A

altering physical barriers and altering immune system barriers

99
Q

How does the viral infection alter the physical barriers ?

A

may damage lung epithelia (virus and immune response); neuraminidase thins mucus and exposes receptors onf epithelial cells- increased bacterial infectivity

100
Q

How does influenza alter the immune response?

A

inhibit neutrophilia

101
Q

When does bacterial coinfection tend to happen with viral infections?

A

later stages of viral infection- during dampening of immune repsonse e.g IL10 upregulation can lead to increased bacterial infection; general downregulation of pathogen sensing following viral infection

102
Q

Why do infants have a tendency towards hyporesponsive immune responses?

A

critical to survive exposure to previously unseen nonpathogenic antigens of both self and foregin origins

103
Q

what type of Th response are infant immune responses skewed towards and why?

A

Th2- reflection of pregnancy- to avoid rejection, Th1 in pregnnacy is associated with preeclampsia, infections eg chlamydia which stimualte Th1 assoc. with abortion

104
Q

Which respiratory viruses have an associated with later-life wheezing?

A

hMPV; RV and RSV

105
Q

What virus is ribavirin used for?

A

RSV

106
Q

What is the problem with antivirals in general?

A

very prone to inducing viral escape mutatns eg oseltamivir resistnace only requires a single point mutation

107
Q

Give an example of passive immunisation?

A

palivizumab- monoclonal antibody against RSV

108
Q

If infants have immune hyporesponsiveness, how is there a problem with immunopathology?

A

have reduced IFN and th1 responses; with increased IL23 and Th17; reduced immunoregulation(IFN increases IDO); lack of previous exposure to virus- increased viral load–resulting response is greater

109
Q

What should be considered with the possiblity of vaccinating against viral infections early in life?

A

infection is important in the development of normal immune responses thereofre vaccination coverage may have an impact on immunity development and more severe infection/asthma later in life

Module 2 (38 decks)

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